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E-MTAB-7315

ABSTRACT: RNA-seq analysis of colonic intestinal epithelial cells (IECs) isolated from naive wild-type C57BL/6 mice, DSS-treated wild-type C57BL/6 mice, Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion

PROVIDER: E-MTAB-7315 | ExpressionAtlas | 2019-01-16

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-7315-analysis-methods.tsv	Tabular
	E-MTAB-7315-analytics.tsv	Tabular
	E-MTAB-7315-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-7315-configuration.xml	Xml
	E-MTAB-7315-g4_g1-mvaPlot.png	Other

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RNA-seq analysis of colonic intestinal epithelial cells (IECs) isolated from naive wild-type C57BL/6 mice, DSS-treated wild-type C57BL/6 mice, Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion

Project description:The aim of this study is to compare the transcriptomic profile of colonic intestinal epithelial cells (IECs) at steady-state, and in several models of colitis: in naive wild-type C57BL/6 mice, in wild-type C57BL/6 mice treated for 7 days with 3% dextran sodium sulfate (DSS) in drinking water, in Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion. Colonic IECs were isolated and FACS-sorted, then subjected tu bulk RNA-seq.

2019-09-30 | E-MTAB-7315 | biostudies-arrayexpress

Project description:RNA-seq analysis of colonic intestinal epithelial cells (IECs) isolated from naive wild-type C57BL/6 mice, DSS-treated wild-type C57BL/6 mice, Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion

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p38a-dependent gene expression in the colonic mucosa

Project description:Gene expression in the colonic mucosa of wild-type and p38a-knockout intestinal epithelial cells (IECs) were compared. C57BL/6 wild-type mice, and intestinal epithelial cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of colonic mucosa

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p38a-dependent gene expression in the colonic mucosa

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Genome-wide mRNA expression profiling for Wild Type and Itch-/- colonic mucosa Transcriptomes by RNA sequencing

Project description:To test the hypothesis that defects in the termination of inflammatory signaling led to colon inflammation, we isolated RNA from the colonic mucosa of Itch-/- mice and from the colonic mucosa of wild-type mice treated with DSS and performed genome-wide mRNA expression profiling by RNA sequencing.

2016-06-20 | GSE81066 | GEO

RNA sequencing data of intestinal tissue from wild-type C57BL/6 mice and ITGB6-overexpressing transgenic mice

Project description:To acquire a better understanding of the role of ITGB6 in the development of inflammatory bowel disease (IBD), we performed mRNA-Req to compare gene expression in two kinds of mice (wild-type C57BL/6 mice and ITGB6-overexpressing transgenic mice) in DSS-induced intestinal fibrosis model.

2024-11-01 | GSE188361 | GEO

Gene expression analysis in Tyk2 deficient AOM/DSS colorectal tumors in mice

Project description:The goal of this study was to determine differences in gene expression profiles in colonic tumors of AOM/DSS treated mice with a total (Tyk2KO) or conditional deletion of Tyk2 in the intestinal epithelium (Tyk2DIEC).

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Immunoregulatory actions of T cell PPAR g at the colonic mucosa

Project description:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. METHODS: Wild-type (WT) or PPAR g flfl; CD4 Cre+ (CD4cre) mice in a C57BL/6 background were challenged with 2.5% DSS in their drinking water for 0, 2, or 7 days. Mice were scored on disease severity both clinically and histopathologically. Flow cytometry was used to assess lymphocyte and macrophage populations in the blood, spleen, and mesenteric lymph nodes (MLN). Global gene expression in colonic mucosa was profiled using Affymetrix microarrays. RESULTS: Both disease severity and inflammation-related body weight loss were accelerated by the deficiency of PPAR g in T cells. Examination of colon histopathology revealed significantly greater epithelial erosion, leukocyte infiltration, and mucosal thickening in the CD4cre mice on day 7. CD4cre mice had more CD8+ T cells than wt mice and fewer CD4+FoxP3+ regulatory T cells (Treg) and IL10+CD4+ T cells in blood and MLN, respectively. Transcriptomic profiling revealed around 3000 genes being transcriptionally altered as a result of DSS challenge in CD4cre mice. These included up-regulated adhesion molecules on day 7 and proinflammatory cytokines interleukin-6 (IL-6) and IL-1b, and suppressor of cytokine signaling 3 (SOCS-3) mRNA expression. CONCLUSIONS: These findings suggest that T cell PPAR g down-regulates inflammation during DSS colitis by inhibiting colonic expression of inflammatory mediators and increasing MLN Treg. Colonic mucosa from wt and CD4cre mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis

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Project description:Group 2 innate lymphoid cells (ILC2) are enriched in colonic tissues, but their precise role under intestinal inflammation, including inflammatory bowel disease (IBD) other than helminth infection, is poorly understood. Here, we analysed global gene expression of colonic ILC2 in healthy and colitis mice and found that type I interferon (T1IFN)-stimulated genes (ISGs) are enriched in ILC2 under DSS-induced colitis. Enhancement of T1IFN signaling in ILC2 under DSS-induced colitis were correlated to downregulation in cytokine production of ILC2, such as IL-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis both in wild-type and Rag2-deficient mice. Collectively, these findings show the potential roles of T1IFN in ILC2 contributing to the development of colitis.

2022-09-21 | GSE212939 | GEO

Transactivation of EGF receptor in intestinal epithelial cells by 2’-fucosyllactose mediates prevention of colitis in adulthood

Project description:2’-fucosyllactose (2’-FL) is a unique oligosaccharide in human milk. We previously reported that 2’-FL protected intestinal integrity, modulated the gut microbial metabolism, and ameliorated intestinal inflammation in adult mice. This study aimed to elucidate mechanisms underlying the direct effects of 2’-FL on intestinal epithelial cells (IECs) for preventing colitis in adulthood. We found that 2’-FL transactivated EGFR in a colonic epithelial cell line, which required 2’-FL-stimulated release of HB-EGF from the cell membrane. Further, findings of 2’-FL-stimulated ADAM17 kinases activity on the cell surface and docking site of 2’-FL to the metalloprotease domain of ADAM17 suggest that 2’-FL could enhance ADAM17 shedding activity for releasing HB-EGF. Remarkably, apoptosis and disruption of tight junction induced by a proinflammatory cytokine and oxidative stress were mitigated by 2’-FL in wild-type, but not EGFR knock-out cell line and colonoids. By using the murine model of colonic injury and colitis induced by DSS, 2’-FL treatment prevented colitis, decreased epithelial apoptosis, and preserved intestinal barrier in wild-type adult mice. These effects were diminished in mice with EGFR deletion in IECs. This study demonstrates a novel mechanism underlying the direct transactivation of EGFR in IECs by 2’-FL that mediates protection of IECs during intestinal inflammation in adulthood.

2025-08-15 | GSE280377 | GEO

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